Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
MAVS Double Nickase Plasmid (h): sc-400769-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MAVS Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- MAVS Double Nickase Plasmid (h) and MAVS Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MAVS. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MAVS Antibody (E-3): sc-166583
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MAVS Double Nickase Plasmid (h) | sc-400769-NIC | 20 µg | $410.00 | |||
MAVS Double Nickase Plasmid (h2) | sc-400769-NIC-2 | 20 µg | $410.00 |
MAVS (mitochondrial antiviral-signaling protein) is a mitochondria-associated adaptor that links cytosolic viral RNA sensing by RIG-I (DDX58) and MDA5 (IFIH1) to downstream innate immune signaling. Upon activation, MAVS nucleates signaling complexes that drive TBK1/IKKε-dependent IRF3/IRF7 activation and canonical IKK-mediated NF-κB signaling, inducing type I interferons and pro-inflammatory cytokines. MAVS activity is regulated by mitochondrial dynamics and post-translational modifications, integrating cellular stress responses with antiviral defense. Dysregulated MAVS signaling has been implicated in altered antiviral susceptibility and inflammatory phenotypes relevant to infection biology and immune-mediated disease mechanisms.
MAVS Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MAVS locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MAVS. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt MAVS function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of MAVS-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.